| Cyproheptadine Hcl | * S in tricyclic ring is replaced by -cH=cH- and N replaced by Sp2 C atom (bioisosterism) *cpd has both H1 antagonist and antiserotonin activity and in pruritis | peptidoleucotriene | *local productn of PLT is major factor in the pathogenisis of asthma *+ PLT leads to 1-constriction of bronchial asthma muscles 2-+ productn of bronchial mucous |
| Ketotifen (Zadifen) | *used as prophylactic so its max action after taken for several weeks) *ttt of asthma by action on mast cells *substit of Cl at 7 position + activity (exception) *it is potent H1 antagonist | Pemitolast | *it is peptidoleucotriene antagonist *used in prophylactic & chronic ttt of asthma |
| Azatidine | *lower CNS effect *ttt of allergic rhinitis *most potent analogue of this series (1st) | Histamine H2 receptor antaginists 1-Cimitidine (tagamet) | *not used now as it has side effects :1-anti- androgenic activity (gynecosmatia ) 2-inhibit cytochrome P450 *should contain NH gp free not subst ,contain guanido gp |
| 2nd generation | due to main side effects of 1st generation is sedation | Ranitidine (Zantac) | *isosteric antaginist of Climitidine by furan instead of imedazole *N is subst ehydrophilic gp but still antagonist (exception) *4-10 times more potent than Cimetidine *not taken e antacid before it 1h or after |
| Terfenadine (Clistadine) | *its side effectss >cause cardiac arrthmia due to acummulatn in body when taken e Macrolides and Ketoconazole as they () metabolism of it *it has no CNS side effects | Nizatidine | *exception :contain hydrophilic gp on N but still antagonist *it is isoteric isomer by thiazole * 5-8 as potent as cimitidine |
| fexofenadine (Allerfen) | *it is ametabolite of Terfenadine *so no problems in metab | Farmotidine | |
| Astimazole | *resemble clemizole in structure (benzimedazole) *it has long duration due to its metab (2 pathways ,either by demethylation or hydroxylation ) and both have antihistaminic activity | drugs acting by other actionrather than H2 receptor blockage : A-Proton Pump inhibitors (PPIs) 1-Omeprazole (losec) | *mech of action of PPIs > block KHATPase (as block SH of enz) >no change in H & K in stomach so (_) acid secretion *it is prodrug w activeted in acid PH *it is formulated in sustaied release enteric coating tablet >to reach parietal cells as it is (pro) *in acid PH it changed to spiro cpd >sulfinic a==sulfinamide >e ATPase >disulfide (inactive enz)] |
| Loratidine (Claritine) | *hydrophobic analogue of Azatidine by addn of aryl chloro gp *derived from basic pipredine gp e neutral carbamate ester >() CNS effect *it has long duration of action | 2-Lansoprazole | disadv :1-gastric carcinod due to excessive use od PPIs >irreversily inhibition of enz (now use reversible inhibition products) adv:no interferance can be taken before and after meals |
| inhibition of mediator release | mediators cause anaphylaxis (block H1 receptor) | B-chemical complexation eg Sucralfate | local binding e ulcer >differential binding to ulcer site form protective barrier prevent exposure of ulcer to acid & pepsin also :it absorbs pepsin and bile salts *side effects :constipation |
| Cromolyn sodium (Intal) | *drug is prophylactic not histamine antagonist ,it prevent release of histamine ,SRSA (slow releasing subs of anaphylaxis) from sensitized mast cells after antigen- antibody reaction | H3 receptor antagonists Thioperamide | H3 antagonists play role in regulatory system not only release and syn of histamine but also release of other neurotransmitters |
| Nedocromil sodium | unlike the relationship of the arylrings in H1 antagonists ,coplanarity of the 2 chromone rings is the most important req for biological activity in the Bis (chromone) series *drug adminst by inhalation as prophylactic and ttt of asthma | H3 receptor agonists 1-Imetit 2-immepip 3-N-methyl histamine | |